Summary and the Future of the Role of C75 in the Treatment of

Obesity

C75 acts through AMPK to decrease appetite in the hypothalamus by altering

fatty acid metabolism

• C75 increases metabolism in the hypothalamus by increasing fatty acid oxidation
• C75 decreases fatty acid synthesis by inhibiting fatty acid synthase
• Subsequent changes in ATP levels modulate AMPK
• AMPK and neuropetides that effect appetite interact
• orexigenic signal, ghrelin, caused an increase in active AMPK
• anorexigenic signal, leptin, caused a decrease in active AMPK
• C75 decreases food intake without activating starvation pathways

  The Future

New papers about C75, the role of AMPK in appetite, and appetite control in the hypothalamus are abundant. C75 is a very promising compound in the fight against obesity. However, specificity and effects in humans are a concern. Since C75 modulates AMPK and neuronal activity, it likely modulates many other cellular processes as past obesity therapeutics have in the past. Studies about its specificity need to be done. Despite of this the major problem with C75, as with other current solution to obesity, is whether a "diet pill" is the solution to our weight problem. Do people eat because they are hungry? Or, are obesity, Syndrome X, and Type-2 Diabetes a consequence of the society we live in? In any case, research like that presented in this report is important in understanding the mechanism and biochemistry of how our brain controls what we do.

[Intro]   [ C75 and Fatty Acid Metabolism]   [AMPK and Neuropeptides]   [C75 and Neuropeptides]   [Discussion]   [References]